DESCRIPTION: This project is aimed at understanding the mechanisms that underlie SINE movement in the mammalian genome. The majority of SINE elements are incapable of efficient amplification, so that the bulk of amplification is dominated by a very few "master" elements. These active elements are the focus of the current proposal. Model systems include the rodent BC1 gene, which is the ID master sequence, as well as primate Alu and rodent B2 repeats. There are four specific aims: 1) To understand why select SINE loci are capable of active transcription and others are not; 2) To understand the role of different portions of the SINE transcript in the stability of the RNAs; 3) To understand the potential role that RNA-protein interactions play in the stability, transport, and potential amplification of SINEs; 4) To develop a tissue culture system in which to measure the retrotransposition rate from either endogenous Alu elements or exogenously added constructs which have been engineered to increase their retrotransposition rates based on the results of the earlier specific aims. To use this system to study the environmental, genetic and physiological factors that influence SINE mobility.